Our data suggests that in normotensive humans cardiopulmonary mechanoreceptors participate in the regulation of renin release. The cardiopulmonary blood volume, through its relationship to the stretch of cardiopulmonary mechanoreceptors, appears to be the "effective" intravascular volume for regulation of renin release. These results provide the background to postulate a hypothesis about the observation that some patients with low-renin hypertension have a normal total blood volume but maintain a larger cardiopulmonary blood volume. The low renin in these patients may stem from suppression of the renal sympathetic tone by volume-stimulated cardiopulmonary receptors. In this investigation, patients' and control subjects' renin status will be classified in various states of sodium balance. Relationship between the intravascular volume distribution, hemodynamics and renin values will be investigated. Acute changes in venous return will be induced by tilting and by placing tourniquets on thighs and the humoral responses analyzed. Hemodynamic and hormonal responses to dietary sodium depletion will also be investigated. Finally, we will investigate whether low renin and high cardiopulmonary blood volume can be found in very early phases of hypertension. This investigation may elucidate the mechanism of renin suppression in some patients with low-renin hypertension and may define the contribution of volume factors to overall control of renin in healthy and hypertensive individuals.